Objective: We wish to test the hypothesis that the septal cholinergic innervation to the hippocampus regulates alpha adrenergic receptor number, and that increased alpha adrenergic receptors are directly involved in the sympathetic sprouting seen in the hippocampus following damage to the septal-hippocampla pathway. We base this hypothesis on our preliminary findings that cholinergic but not adrenergic neuronal lesion leads to a specific increase to alpha adrenergic receptors but not beta adrenergic, muscarininc or nicotinic cholinergic, opiate or benzodiazepine receptors. This receptor increase precedes the sprouting response of sympathetic nerve terminals which we have previously well documented. Scientific Methods: Radioreceptor assays for neurotransmitter receptors, light and fluorescence microscopy, autoradiography, intracerebral injection of neurotoxins, electrolytic and mechanical lesions, acute and chronic treatment with cholinergic and adrenergic agonists and antagonists. Significance: Neurotransmitter receptor alteration may serve as a general mechanism controlling synaptic growth and plasticity throughout the brain during development and maturity. Receptors number can be modulated pharmacologically and thus such intervention may be able to indirectly modulate synaptic connectivity. Neuronal sprouting and synaptic plasticity may underlie memory formation. The understanding of such receptor mediated processes may lead to a clearer appreciation of the mechanisms involved in both neuronal growth during development and in memory formation.